Management of a retained catheter in an arteriovenous malformation. Case report

The long-term effects of retained catheters in patients are not well known; therefore, the clinical presentation may differ. The authors present the case of a 21-year-old man with a pseudoaneurysm of the left common femoral artery, which developed 3 months after a transfemoral microcatheter embolization of a cerebral arteriovenous malformation (AVM) in which the catheter was inadvertently glued into the AVM and was retained at the groin.     

Antioxidant responses and metal accumulation in tissues of Nile tilapia Oreochromis niloticus under Zn,Cd and Zn + Cd exposures

We investigated the effects of Zn, Cd and a Zn + Cd mixture on antioxidant parameters and metal accumulation in Oreochromis niloticus. Fish were exposed to 0.5 and 5.0 mg l^?1 Zn, 0.1 and 1.0 mg l^?1 Cd, and 0.5 mg l^?1 Zn + 0.1 mg l^?1 Cd and 5.0 mg l^?1 Zn + 1.0 mg l^?1 Cd mixtures for 7 and 28 days to determine Zn and Cd accumulation, reduced glutathione (GSH) level and glucose‐6‐phosphate dehydrogenase (G6PD) activity in gill and liver. There was increasing accumulation of the metals in the tissues with increasing concentrations of metals in the exposure medium and with increasing duration of exposure (except at the lower concentration of Zn). Concentration of metals in the tissues of fish exposed to the Zn + Cd combination were significantly lower than in fish exposed to the single metal. The highest metal accumulation was observed in the liver. Exposure to the heavy metals affected the antioxidant parameters in the tissues, with both GSH level and G6PD activity in the gill and liver being increased under Zn, Cd and Zn + Cd exposures, especially in their higher concentrations. These increases in the antioxidant responses were higher with the Cd alone, and in combination with Zn, than with Zn alone. Furthermore, GSH level and G6PD activity increased with increasing exposure period only for Cd alone, and in Cd combination with Zn. The results indicate that O. niloticus resisted oxidative stress induced by heavy metal exposure by antioxidant mechanisms. Copyright © 2008 John Wiley & Sons, Ltd.     

Increased myocardial collagen turnover in patients with progressive cardiac conduction disease

Background: Histopathologically, progressive cardiac conduction disease (PCCD) is characterized by progressive fibrosis and sclerodegenerative changes in the proximal and distal conduction system of the heart. Therefore, we sought to determine the serum levels of myocardial collagen turnover markers, extracellular matrix components, transforming growth factor β₁ (TGFβ₁), and bone morphogenic protein‐7 (BMP‐7) in this population. Methods: Study population included 20 patients (6 M/14 F, mean age 76 ± 8 years) with acquired, permanent 2:1, or complete atrioventricular block and compared with age‐ and sex‐matched, asymptomatic, healthy control subjects (n = 18, 6 M/12 F, mean age 75 ± 7 years). Serum myocardial collagen turnover markers:matrix metalloproteinases (MMP‐1, 2, 9), tissue inhibitor of matrix metalloproteinase (TIMP‐1), amino‐terminal propeptide of procollagen type I (PINP) and type III (PIIINP), carboxy‐terminal telopeptide of collagen type I (CITP), and carboxy‐terminal propeptide of procollagen type I (PICP), serum extracellular matrix components (laminin and fibronectin), TGFβ₁, and BMP‐7 levels were measured in both groups. Results: Serum PICP (849 ± 396 vs 631 ± 294 ng/mL, P = 0.04), PIIINP (3.7 ± 1.3 vs 3 ± 1 μg/L, P = 0.03), CITP (0.68 ± 0.35 vs 0.48 ± 0.25 ng/mL, P = 0.037), and plasma MMP‐9 (58.8 ± 56 vs 25.9 ± 17.3 ng/mL, P = 0.006) levels were higher in patient population compared to control subjects. Serum MMP‐1 (24.1 ± 20.5 vs 13.6 ± 7.5 ng/mL, P = 0.045) and MMP‐2 (1310 ± 139 vs 1186 ± 163 ng/mL, P = 0.01) levels were higher in control subjects compared to patient population. There was no difference in serum TIMP‐1, PINP, laminin, fibronectin, TGFβ₁, and BMP‐7 levels between two groups. Conclusion: Our findings demonstrate the presence of increased myocardial collagen turnover and active fibrotic process in patients with PCCD compared to control subjects.     

Is microRNA 1910-3p (miR-1910-3p) a really distinctive marker for psoriasis?

Background/aimAlthough the cause of immune activation in the pathogenesis of psoriasis is still unclear, miRs are thought to have an effect on psoriasis. This work aimed to evaluate the role of miRs (miR-4649-3p, miR-6867-5p, miR-4296, miR-210, and miR-1910-3p) that target the FOXP3 mRNA and IL-17A mRNA in psoriasis. Materials and methods Forty-four psoriasis patients and 44 healthy controls were included in the study. Quantitative real-time PCR (qRT-PCR) was used for the measurement of miRs. Serum IL-17A levels were determined by an enzyme-linked immunosorbent assay (ELISA) method. Results Plasma miR-1910-3p levels were significantly lower in the patient group than the controls (P = 0.000, fc: 0.10). ROC analysis showed that plasma miR-1910-3p levels could significantly differentiate psoriasis patients from healthy controls [AUC = 0.912 (0.848–0.975), P = 0.000]. The plasma miR-4649-3p level was significantly higher in the psoriasis group compared to the controls (P = 0.000, fc: 2.99). Conclusion Decreased expression of miR-1910-3p increases the risk of developing psoriasis by approximately 50-fold and was able to use for the significant differentiation of psoriatic patients from healthy controls.     

Poly (ADP-ribose) polymerase as a potential target for the treatment of acute renal injury caused by lipopolysaccharide

Recent studies have clearly reported that there is a relationship between endotoxemia and acute renal injury. The aim of this study was to investigate whether treatment with the new potent PARP inhibitor PJ34 could prevent the acute renal injury induced by lipopolysaccharide (LPS). Endotoxemia was induced by LPS injection (10 mg/kg, i.v.). LPS increased blood urea nitrogen (BUN) levels from 22 +/- 0.54 mg/dL to 45.7 +/- 5.79 mg/dL (p < 0.05). The plasma creatinine levels were 0.38 +/- 0.02 mg/dL and 0.47 +/- 0.03 mg/dL for the control and LPS groups, respectively. In addition, urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular damage) was increased after LPS injection. By light microscopy, structural renal damage was observed in the LPS-treated group. However, PJ34 treatment (10 mg/kg, i.p.) attenuated LPS-induced renal injury, as indicated by plasma BUN and creatinine levels, urinary NAG excretion, and renal histology. These results indicated that the overactivation of the PARP pathway may have a role in LPS-induced renal impairment. Hence, pharmacological inhibition of this pathway might be an effective intervention to prevent endotoxin-induced acute renal injury.     

An atypically localized atrial myxoma: a case report

Atypical cardiac myxomas are rare occurrences and may present with a variety of clinical manifestations depending on the location and morphology. A 46-year-old woman had a 4 x 3 x 2-cm myxoma originating from the superior wall of the left atrium, found by echocardiography and multislice tomography. The tumor was successfully treated by surgical excision. The resected tumor was a well-defined encapsulated mass with a narrow-base stalk originating from the right wall of the left atrium in between the right upper and lower pulmonary vein. The patient recovered without complication and was discharged 6 days after the operation. At 1-year follow-up, echocardiography revealed normal cardiac function without reccurence in terms of mass. Although up to 80% of myxomas are localized in the left atrium, of which 75% involve in the interatrial septum, it should not be forgotten that myxomas can appear in an atypical localization, as occurred in our case.     

Circulating platelet–leukocyte aggregates in patients with inflammatory bowel disease

BackgroundInflammatory bowel diseases (IBDs), Crohn's disease, and ulcerative colitis are considered to be chronic inflammatory disorders implicated with recurrent tissue damage to the intestine. There is a positive correlation between platelet–leukocyte aggregates and ischemic vascular risk. There are limited data about the relationship between platelet–leukocyte aggregates and IBD. This study was designed to determine whether platelet–leukocyte aggregates increase in IBD, and whether a relationship exists between the elevation of platelet–leukocyte aggregates and disease activity.MethodsA total of 20 patients with IBD (16 with ulcerative colitis and 4 with Crohn's disease) and 20 healthy controls participated in our study. Nine patients were in active-phase IBD, whereas 11 patients were in inactive phase. To show the presence of thrombocyte aggregates, the monoclonal antibodies such as Isotype IgG1 mouse antihuman CD42b-PE (phycoerythrin) (Beckman Coulter IMI417), Isotype IgG1 mouse antihuman CD45-FITC (fluorescein isothiocyanate) (Beckman Coulter IM0782), and Isotype IgG2a mouse antihuman CD45RO-FITC (Beckman Coulter IMI247) were used. Additionally, the values of platelet–neutrophil aggregates were measured in peripheral blood samples using flow cytometry techniques.ResultsThe levels of platelet–leukocyte aggregates in blood samples were found to be significantly higher during both the active and inactive phases in patients with IBD. There were no statistically significant differences between active-phase and inactive-phase patients.ConclusionWe determined that the patient group had significantly higher platelet–leukocyte aggregate levels compared with the control group. This finding suggests that platelet–leukocyte aggregates may play a role in the development of IBD.     

Bullous pemphigoid and cholestatic hepatitis associated with Castleman's disease.

The case of a 21-yr-old woman admitted with a two-week history of icterus, fever, multiple peripheral lymphadenopathy and pruritic eruption is presented. A full evaluation including computed tomography, endoscopic retrograde cholangiography, liver, skin and lymph node biopsies and biochemical tests confirmed the diagnosis of multicentric Castleman's disease (angiofollicular lymph node hyperplasia). All symptoms improved within four weeks of commencing prednisone therapy. Castleman's disease should be considered in the differental daignosis of cholestatic hepatitis and bullous pemphigoid.     

Excitability of facial nucleus and related brain-stem reflexes in hemifacial spasm, post-facial palsy synkinesis and facial myokymia.

OBJECTIVE: To compare the electrophysiological excitability characteristics of the facial nucleus and related structures in hemifacial spasm (HFS), post-facial palsy synkinesis (PFPS) and facial myokymia (FM). METHODS: Facial F-waves, blink reflex recoveries and magnetically elicited silent periods (SP) were prospectively studied in 17 HFS, 17 PFPS, 8 FM cases and in 13 controls. Earlier unpublished observations on abnormal impulse transmission in 36 HFS and 29 PFPS cases were also included. RESULTS: Enhanced F-waves were recorded on the symptomatic side in PFPS and HFS cases with a tendency to be more pronounced in PFPS. HFS and PFPS groups both showed an earlier blink reflex recovery, more prominent in PFPS patients, when stimulated and/or recorded on the symptomatic side. Unelicitable SPs were encountered after 24/39 stimulations in 5 patients with PFPS and rarely in HFS cases. Duration of elicitable SPs did not change remarkably. FM group had similar characteristics as normal controls in the 3 electrophysiological tests. Latencies of the lateral and synkinetic spread responses were significantly prolonged in the earlier PFPS group as compared to HFS. In two-point stimulation, both groups showed a greater latency shift in late responses, again more pronounced in PFPS. CONCLUSIONS: PFPS and HFS cases had similar enhanced excitability patterns at the facial nucleus and related brain-stem structures, more marked on the symptomatic side and more obvious in the PFPS group. Findings elicited in the FM group were thought to be caused by asynchronous hyperactivity of facial motoneurons. SIGNIFICANCE: In this comparative electrophysiological study, similar excitability patterns were found in HFS and PFPS groups, albeit with different intensities.     

Does Obstructive Sleep Apnea Increase the Risk for Periodontal Disease? A Case‐Control Study

Background: A possible association between periodontitis and obstructive sleep apnea (OSA) has been suggested. The aim of this study is to compare periodontitis prevalence between controls and patients with OSA by assessing clinical periodontal parameters and gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β, tumor necrosis factor (TNF)‐α, and high‐sensitive C‐reactive protein (hs‐CRP); serum hs‐CRP was also sampled. Methods: A case‐control study was performed that included 163 individuals: 83 individuals (18 females and 65 males) with OSA and 80 non‐OSA individuals (23 females and 57 males) as controls. The test group was classified according to OSA severity. Clinical periodontal measurements were recorded, and GCF samples were collected. GCF hs‐CRP, IL‐lβ, and TNF‐α levels were analyzed using an enzyme‐linked immunosorbent assay method. Serum hs‐CRP was measured by latex‐enhanced immunoturbidimetric assay. Results: Prevalence of periodontitis in the OSA group (96.4%) was significantly higher than in the control group (75% [P <0.001]). Severe periodontitis prevalence was higher in the OSA group than control group. All periodontal clinical parameters and GCF IL‐lβ concentrations were significantly higher in patients with OSA than in controls (P = 0.001). No significant differences were found between the mild OSA and moderate‐to‐severe OSA groups. Additionally, there was no significant difference in GCF TNF‐α and hs‐CRP levels between the groups (P >0.05). Serum hs‐CRP levels were significantly higher in patients with OSA. A significant correlation was found between GCF IL‐1β and all clinical parameters. Conclusions: Results demonstrated higher prevalence of periodontitis and higher levels of GCF IL‐1β and serum hs‐CRP in patients with OSA. However, there is still a need for randomized clinical trials testing oral care interventions.